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Researchers Discover a Control Switch That Serves to Relieve Cellular Stress

Posted by MullanMichael on August 04, 2015

Researchers Discover a Control Switch That Serves to Relieve Cellular Stress

A new discovery by University of San Diego researchers could be the key to opening new doors of understanding and treating a number of neurodegenerative disorders such as, Alzheimer’s, Parkinson’s, and ALS, as well as diabetes, cancer and inflammatory disorders. The ramifications are significant and could vastly improve the process of developing new drug therapies to treat these conditions.

Cell death

The normal process when the body undergoes stress is that the endoplasmic reticulum, where all proteins are stored and shaped, experiences a buildup of unfolded or not properly folded proteins. In order to function properly, proteins must be three-dimensional. When there is stress, the protein shaping process is impacted, producing misshapen proteins. The unfolded protein response (UPR), a cellular stress relief mechanism, senses the problem, and begins to correct the cellular process. If not successful, then the UPR sends a signal to the cell to destroy itself.

A new control switch for the unfolded protein response (UPR) 

According to the study published in EMBO Reports by researchers at the University of California, San Diego School of Medicine, two pathways are involved in cell stress response, the UPR and a nonsense-mediated RNA decay pathway (NMD). Dr. Miles, senior author of the paper, said that the two pathways intersect at some point when there is cell stress, indicating that NMD acts to control UPR so that it does not overreact to mild stress.

Diseases such as cancers, diabetes, Parkinson’s and Alzheimer’s are known to cause significant cell stress at a level that typically triggers a self-destruct signal from the UPR. Without a control mechanism, the resulting acceleration of cell death can lead to a rapid deterioration in the health of the patient. According to the researchers, the intersecting NMD is crucial to normalizing the UPR activities, thus protecting the patient from extreme levels of cell death.

 

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